Avaliação da proteção gástrica e duodenal do monoterpeno nerol em roedores
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Data
2012-05-03
Autores
Angelis, Célio Damacena de [UNESP]
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Universidade Estadual Paulista (Unesp)
Resumo
Este projeto se propôs a avaliar a ação farmacológica do nerol na prevenção de úlcera péptica. Nerol na dose de 60 mg/Kg por via oral exerceu proteção contra lesão gástrica induzida por etanol e por droga anti-inflamatória não esteróide (DAINE) em ratos, mas não protegeu contra úlcera duodenal induzida por cisteamina. Experimentos foram realizados para a elucidação dos mecanismos ação e verificou-se que a proteção exercida pelo Nerol não é por bloqueio dos radicais livres, por redução da secreção gástrica ou por aumento de muco, sua ação também não ocorre por formação de barreira mecânica. Verificou-se, contudo, que houve redução da motilidade gastrointestinal, o que pode ser um indicativo de redução do esvaziamento gástrico, o que contribui para o efeito gastroprotetor. A redução da motilidade gastrointestinal assim como a redução do acúmulo intestinal exercido pelo nerol foi revertida pela administração de naloxona (antagonista de receptores opióides), indicando, portanto, o envolvimento destes receptores. Através do bloqueio de fatores protetores da mucosa gástrica, verificou-se que a gastroproteção exercida pelo nerol é independente da via do óxido nítrico, de prostaglandinas e dos receptores mu opióides, porém, é dependente de compostos sulfidrílicos. Mostrou-se através da quantificação dos níveis de glutationa (GSH) e da atividade da enzima mieloperoxidase (MPO) que o tratamento com nerol mantém os níveis de compostos sulfidrílicos não-protéicos e reduz a infiltração de neutrófilos na mucosa gástrica em animais com lesão gástrica induzida por etanol. A administração aguda de nerol (doses de 60, 300, 600, 1250, 2500 ou 5000 mg/Kg) não provocou mortes nem alterações significantes nos parâmetros comportamentais até a dose de 600 mg/Kg. Neste trabalho portanto, ficou...
The present project proposed to evaluate the pharmacologic action of nerol in the prevection of peptic ulcer. It was seen that 60 mg/kg (p.o.) of nerol prevented gastric lesions induced by ethanol and no steroidal anti-inflammatory drugs (NSAID) in rats, however nerol did not have protected duodenal mucosa against cysteamine. Assays were performed to elucidation of the mechanisms of action and it was found that protection exerted by Nerol does not by block of free radicals, nor decrease gastric acid secretion nor increase mucus, its action is not by create a mechanical barrier. However It was found that nerol reduced gastrointestinal motility, this might be an indicative of slower gastric emptying that contribute to the gastric protective effect. Reduction of gastrointestinal motility, as well as the reduction of intestinal accumulation exerted by nerol was reverted by naloxone administration (antagonist of opioid receptors), therefore indicating involvement of the cited receptors. By blocking protective factors of gastric mucosa, it was verified that nerol’s gastroprotective effect does not involve nitric oxide, prostaglandin nor mu opioid receptors, but is dependent of sulfhydryl compounds. It was shown by quantifying glutathione levels (GSH) and myeloperoxidase (MPO) action that treatment with nerol keeps the levels of non proteic sulfhydryl compounds and decreases the neutrophil infiltration into the gastric mucosa in animals with ethanol-induced gastric damage. Acute administration of nerol (60, 300, 600, 1250, 2500 and 5000 mg/Kg) presented no deaths, neither significant behavior changes to doses of 60, 300 and 600 mg/kg. In this work, nerol showed a gastroprotective effect against ethanol- and indomethacin-induced lesions, and the depence of sulfhydryl compounds. The involvement of opioid receptors and the gastrointestinal... (Complete abstract click electronic access below)
The present project proposed to evaluate the pharmacologic action of nerol in the prevection of peptic ulcer. It was seen that 60 mg/kg (p.o.) of nerol prevented gastric lesions induced by ethanol and no steroidal anti-inflammatory drugs (NSAID) in rats, however nerol did not have protected duodenal mucosa against cysteamine. Assays were performed to elucidation of the mechanisms of action and it was found that protection exerted by Nerol does not by block of free radicals, nor decrease gastric acid secretion nor increase mucus, its action is not by create a mechanical barrier. However It was found that nerol reduced gastrointestinal motility, this might be an indicative of slower gastric emptying that contribute to the gastric protective effect. Reduction of gastrointestinal motility, as well as the reduction of intestinal accumulation exerted by nerol was reverted by naloxone administration (antagonist of opioid receptors), therefore indicating involvement of the cited receptors. By blocking protective factors of gastric mucosa, it was verified that nerol’s gastroprotective effect does not involve nitric oxide, prostaglandin nor mu opioid receptors, but is dependent of sulfhydryl compounds. It was shown by quantifying glutathione levels (GSH) and myeloperoxidase (MPO) action that treatment with nerol keeps the levels of non proteic sulfhydryl compounds and decreases the neutrophil infiltration into the gastric mucosa in animals with ethanol-induced gastric damage. Acute administration of nerol (60, 300, 600, 1250, 2500 and 5000 mg/Kg) presented no deaths, neither significant behavior changes to doses of 60, 300 and 600 mg/kg. In this work, nerol showed a gastroprotective effect against ethanol- and indomethacin-induced lesions, and the depence of sulfhydryl compounds. The involvement of opioid receptors and the gastrointestinal... (Complete abstract click electronic access below)
Descrição
Palavras-chave
Farmacologia, Estomago - Ulceras, Glutationa, Stomach - Ulcers
Como citar
ANGELIS, Célio Damacena de. Avaliação da proteção gástrica e duodenal do monoterpeno nerol em roedores. 2012. 74 f. Dissertação (mestrado) - Universidade Estadual Paulista Julio de Mesquita Filho, Instituto de Biociências de Botucatu, 2012.